期刊
ARCHIVES OF GYNECOLOGY AND OBSTETRICS
卷 303, 期 5, 页码 1175-1183出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00404-020-05844-4
关键词
α vβ 3 integrin; Extravillous trophoblasts; Placenta accreta and villous trophoblasts
The study found significantly elevated expression of alpha v beta 3 integrin in patients with placenta percreta, mainly contributed by EVT cells. This suggests a potential role of this adhesion molecule in pathological placentation.
Background Placenta accreta is one of the most serious complications in obstetrics and gynecology. Villous trophoblasts (VT) and extravillous trophoblasts (EVT) play a central role in normal placentation. Placenta accreta is characterized by abnormal invasion of EVT cells through the uterine layers, due to changes in several parameters, including adhesion proteins. Although alpha v beta 3 integrin is a central adhesion molecule, participating in multiple invasive pathological conditions including cancer, data on placenta accreta are lacking. Objective To study the expression pattern of alpha v beta 3 integrin in placenta accreta in comparison with normal placentas. Study design We collected tissue samples from placentas defined as percreta, the most severe presentation of placenta accreta and from normal control placentas (n = 10 each). The samples underwent protein extractions for analyses of alpha v beta 3 expression by Western blots (WB) and a parallel tissue assessment by immunohistochemistry (IHC). Results WB results indicated significantly elevated alpha v beta 3 integrin expression in the percreta samples compared to normal placentas. These elevated levels were mainly contributed by EVT cells, as demonstrated by IHC. alpha v beta 3 integrin demonstrated a classical membranal expression in the VT cells, whereas a uniformly distributed expression was documented in the EVT cells. These patterns of the alpha v beta 3 integrin localization were similar in both accreta and normal placental samples. Conclusions Enhanced alpha v beta 3 integrin expression, mainly in extra villous trophoblasts of placenta percreta, implies for a role of this adhesion molecule in pathological placentation.
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